Lecture 10: Staphylococcocus aureus Flashcards
What does staph aureus look like under a microscope and why
It is a spherical bacteria that has more than one plane of division so appears as grapelike clusters.
Are Staph aureus gram + or gram -
How does this correspond to stain
As they have a thick peptidogylcan cell wall they are stained purple and are Gram +
What are different ways Staph infection shows itself in skin infection
Cellulitis which is deep skin infection which has searing pain bc of intense inflammatory response
Folliculitis: infection of hair follicles, also presents as furuncles (boils) which is full of pus.
Impetigo: acute skin infection presenting as scablike sores
What is the state of invasive S aureus disease in NZ
S. Aureus is endemic in NZ and its case fatality rate is 20% across all ages, with increased risk for Maori and Pasifika
Where does S. aureus come from
Mainly a human pathogen transmitted human to human but can go human to domestic animals
No environmental reservoir known
What are two types of non human staph aureus diseases
- bovine mastitis which infects udders
- broiler chicken bone and soft tissue infection
What factors contribute to to disease caused by Staph aureus
Through host factors, environmental factors, (bacterial factors not that strong)—> exposure. After that, disease can be caused straight away or Staph colonises the host and can cause it later
What is colonisation of Staph, where does it happen
Colonisation is where the staph bacteria is living on the host but the host doesn’t have symptoms. There are nasal carriers but Staph is also distributed around the body (perineum, skin of abdomen and chest)
What are the different frequencies of colonisation and what determines incidence of colonisation
There are persistent carriers (20%), non carriers (15%) and intermittent carriers (65%).
Peak incidence of colonisation is in the first year of life and declines with old age.
What types of dis-ease does staph cause (% per year)
In most colonised, no symptoms in 60% but food poisoning is common, skin infection is 3% and there are serious infections in any organ, 0.02% per year
Why don’t we get heaps of bacterial infections because there is so many bacteria
Most bacteria on the skin do not interact with human cells, only some have the ability to interact
What are 4 adaptions that Staph aureus has of innate immune resistance
- Coat itself in antibody, clotting proteins (fibrinogen), sugar capsule to avoid being detected/phagocytosed by white blood cells
- Release CHemotaxis Inhibitory Proteins that stops more phagocytes being recruited by blocking their receptors for chemotaxis
- Use Catalase enzyme to break down H2O2 inside the the neutrophil
- Release haemolysin, PVL toxins to destroy neutrophils after engulfment, allowing release to go on to explore further
How does protein A helps the Staph aureus
It binds the immunoglobulins meant to mark the bacteria for destruction on the heavy chain instead of the active site on the light chains by showing the light chains it masks the bacteria
How is S. aureus infections treated
- Person is stabilised
- pus is drained (can be in spine or joints)
- Antibiotics used to kill bacteria
What are the two antibiotic resistance S. aureus and how do they achieve this
- Penicillin resistant SA which produced an enzyme B-lactamase which breaks the B-lactam ring.
- Methicillin resistant SA which changed the structure of the transpeptidase enzyme so it methicillin couldn’t bind at all